991bp deletion that removes the mir-100, let-7 and mir-125 microRNAs. The Scer\GAL4 coding region and a w[+] marker have been inserted in their place. The Scer\GAL4 coding sequence is expressed by transcription from the "let-7-C" promoter (the promoter of the polycistronic transcription unit that normally encodes mir-100, let-7 and mir-125).
The musculature and myoblasts of Df(2L)let-7-CGKI/Df(2L)let-7-CKO1 larvae appear normal.
43% of Df(2L)let-7-CKO1/Df(2L)let-7-CGKI animals die prematurely during the course of development, with 74% of these arresting at the very end of metamorphosis. The remaining 57% of Df(2L)let-7-CKO1/Df(2L)let-7-CGKI animals eclose as adults, but have chronic defects in function, including severely reduced motility, climbing ability, flight and male and female fertility.
The adult neuromusculature of Df(2L)let-7-CKO1/Df(2L)let-7-CGKI animals displays persistent pupal as well as immature adult characteristics. The dorsal internal oblique muscles (DIOMs) that ordinarily decay during post-eclosion maturation fail to disappear in older mutant adults in most cases, and the neuromuscular junctions connecting DIOMs and their innervating motoneurons also fail to decay. The dorsal muscles (DMs) of mutant adults are smaller than those of age-matched controls. The mutant DMs are narrower and contain fewer nuclei compared to wild-type controls. The neuromuscular junctions of the Dms are either completely absent, shorter in length than normal, or devoid of boutons, appearing as long, thin processes along the length of the DM.
In Df(2L)let-7-CGKI mutant adults, the pupal dorsal internal oblique muscles fail to decay, whereas the adult dorsal muscles do not achieve their normal size. Adult flies display defects in motility, flight and fertility.
Associated with: Scer\GAL4let-7-C.
The "let-7-C[GKI]" chromosome carries a 991bp deletion that removes the mir-100, let-7 and mir-125 microRNAs. The chromosome also carries the Scer\GAL4 coding sequence, which is expressed by transcription from the "let-7-C" promoter (the promoter of the polycistronic transcription unit that normally encodes mir-100, let-7 and mir-125).